Tachyarrhythmia is an irregular heartbeat caused by transmission of hyperexcitability to a normal cardiac muscle tissue or formation of a circling circuit (reentry circuit) of electrical excitation in a cardiac muscle tissue. Usually, excitation of the heart is controlled at a normal rate (sinus rhythm) by excitation from the sinoatrial node. In the event of tachyarrhythmia, however, the heart rate at a rate higher than the sinus rhythm persists due to hyperexcitability from some heart tissues. The reentry circuit refers to a portion in which normal transmission of electrical excitation fails to occur, and waves of excitation circulate in a circuit due to the existence of a transmission impairment site in a cardiac muscle tissue or the like. This reentry circuit is involved in persistence of tachyarrhythmia, and occurrence and transmission of hyperexcitability cause an episode of tachyarrhythmia. For example, atrioventricular nodal reentry tachycardia (AVNRT), caused by atrial extrasystoles, is arrhythmia that persists by the formation of a reentry circuit in the atrioventricular node and a portion of the atrium. In the event of this condition, a radical therapy is available in which a portion of the reentry circuit is blocked by catheter ablation or the like. Radical therapies for stopping an attack are performed for the treatment of tachyarrhythmia such as atrial fibrillation (AF) since the cause thereof has been found to exist at a specific site.
For example, atrial fibrillation (AF) is a kind of cardiac arrhythmia and refers to arrhythmia caused by irregular atrial excitation. This condition causes thrombotic diseases such as cerebral infarction. Paroxysmal occurrence of atrial fibrillation is caused by the existence of straying electrical signals from the left atrium (LA) to the pulmonary vein (PV) in a cardiac muscle tissue. In the event of atrial fibrillation, the atrioventricular node receives electrical impulses not only from the sinoatrial node but also from many sites in the whole atrium. The atrioventricular node cannot manage to process these impulses, which results in an irregular and high heart rate. As a result, blood is retained in the atrium, increasing risks of forming thrombi. Examples of the major risk factors for atrial fibrillation include age, coronary arterial diseases, rheumatic heart diseases, hypertension, diabetes, thyrotoxicosis, and so forth. Atrial fibrillation can be treated by interrupting electrical conduction from the pulmonary vein showing focal activity to the left atrium. For example, atrial fibrillation can be treated by catheter ablation, in which a catheter is inserted so that it should reach a portion of the left atrium, and the hyperexcitability conduction pathway is cauterized using high frequency, ultrasonic waves, or the like to necrotize cells in the portion (refer to Patent Document 1 and Non-patent Documents 1 to 4). Examples of the therapy by catheter ablation include balloon catheter ablation using a balloon catheter for treatment with ultrasonic waves or high frequency and the like.
However, since some cells in atrial tissues are necrotized with heat in these conventional catheter ablation therapies, atrial tissues are severely damaged. Furthermore, intense cauterization may cause adverse reactions such as tissue carbonization, thrombogenesis, and perforation of surrounding tissues such as the esophagus.
Therefore, a transmural treatment method that causes a minimal damage to atrial tissues and surrounding tissues and prevents a thermal damage to the atrial tissues has been awaited.
In general, a photodynamic therapy is used in cancer treatment and the like. Application of the photodynamic therapy (PDT, also referred to as photochemotherapy) to various treatments such as endoscopic treatment of early cancer has been considered (refer to Patent Documents 2 and 3). PDT is a therapy in which a photosensitizer such as a specific type of porphyrin derivatives is administered by intravenous injection or the like and selectively absorbed and accumulated in a tissue portion to be treated in which a lesion such as a cancer tissue is observed, and then the lesion is irradiated with a light ray such as a laser beam to destroy the tissue, utilizing properties of photosensitizers of being selectively accumulated in a lesion and being sensitized by a light. Currently, however, the property of being accumulated is not utilized in some therapies. Such a therapy involves a mechanism in which a photosensitizer taken up in a lesion by photoradiation is excited, the energy in the sensitizer is transferred to oxygen molecules existing inside the lesion to generate active singlet oxygen, and the active oxygen kills cells in the lesion by apoptosis or necrosis.
Furthermore, although a photodynamic therapy using a lipid-soluble porphyrin as a photosensitizer and a balloon catheter for the treatment of arrhythmia has been reported (Patent Document 4), specific conditions and the like of the therapy have not been reported.
Patent Document 1: JP Publication (Kokai) No. 2004-130095
Patent Document 2: JP Patent No. 2961074
Patent Document 3: JP Patent Publication (Kohyo) No. 7-53733
Patent Document 4: US Patent No. US2002/0095197
Non-patent Document 1: Carlo Pappone et al., Circulation. 102: 2619-2628 (2000)
Non-patent Document 2: Mathaniel M. Fried et al., Lasers in Surgery and Medicine. 28: 197-203 (2001)
Non-patent Document 3: Kazushi Tanaka et al., Journal of American College of Cardiology. Vol. 38, No. 7, 2079-2086 (December 2001)
Non-patent Document 4: Walid Saliba et al., Journal of Cardiovascular Electrophysiology. Vol. 13, No. 10, 957-961 (October 2002)